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1 ed serum amyloid A production or EPO-induced reticulocytosis.
2 rastingly, produced greater splenomegaly and reticulocytosis.
6 rescent erythrodontia, hemolytic anemia with reticulocytosis and extramedullary erythropoiesis, and,
8 and hemoglobin nadirs and provided enhanced reticulocytosis and faster recovery, compared with contr
10 eductions in Hoxa7(-/-) mice correlated with reticulocytosis and thrombocytopenia without anemia.
11 Peripheral blood counts revealed a profound reticulocytosis and thrombocytosis despite normal serum
12 reased hematocrit and red blood cell counts, reticulocytosis, and bilirubinemia, leading secondarily
13 treated with eculizumab, persistent anemia, reticulocytosis, and biochemical evidence of hemolysis a
14 e of hyperparasitemia, more profound anemia, reticulocytosis, and death 14 to 21 days after infection
15 bly sickled cells in their peripheral blood, reticulocytosis, and other phenotypic features of SCA.
18 topenia, platelet dysfunction, splenomegaly, reticulocytosis, and unbalanced hemoglobin chain synthes
19 and increased RBC turnover with compensatory reticulocytosis, but anemia was not as severe as that in
23 and C-reactive protein) and did not exhibit reticulocytosis during the weeks following discharge.
24 tion; this treatment concomitantly decreased reticulocytosis, erythropoietin abundance and splenomega
25 ly in RBCs and causes microcytic anemia with reticulocytosis, implicating Rac GTPases as dynamic regu
26 ticulocytes are rarely infected, the delayed reticulocytosis in susceptible strains may result from p
30 nt of sickle-associated hemolytic anemia and reticulocytosis, key pathophysiological biomarkers of SC
31 isease associated with significantly greater reticulocytosis, leukocytosis, neutrophilia and thromboc
33 use recovery from anaemia requires transient reticulocytosis, our findings imply that in malarious re
34 y perturbed erythroid development and led to reticulocytosis plus heightened splenic erythropoiesis.
35 Increased levels of circulating Epo lead to reticulocytosis, polycythemia, and suppression of hepati
36 globin levels into the normal range, reduced reticulocytosis, reversal of splenomegaly and up to 7% b
37 displayed microcytic hypochromic anemia with reticulocytosis that was partially compensated by avid e
38 ociated with decreased RBCs volume (MCV) and reticulocytosis; the flow-cytometric assay showed good c
39 s a reflection of parasitemia level, but low reticulocytosis was evident despite differences in paras
40 vated serum IgM or the presence of anemia or reticulocytosis which is mainly seen in response to auto
42 s were well tolerated and appeared to effect reticulocytosis, with a peak at day 11 or 15 in most pat
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